Pyoderma gangrenosum
Pyoderma gangrenosum jẹ́ àìlera ara iredodo níbi tí àwọn pustules tó ń ṣe irora tàbí àwọn nodules ń di ọ̀gbẹ́ tó ń gòkè sí i. Pyoderma gangrenosum kì í ṣe àrùn àkóràn. Ìtọ́jú lè ní corticosteroids, ciclosporin, tàbí oríṣìíríṣìí egboogi monoclonal. Bí ó tilẹ̀ jẹ́ pé ó lè ní ipa lórí ènìyàn ní gbogbo ọjọ́‑ori, ó ṣe pàtàkì jùlọ fún àwọn tó wà ní ọdún 40 sí 50.
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Ninu awọn abajade 2022 Stiftung Warentest lati Jẹmánì, itẹlọrun alabara pẹlu ModelDerm jẹ kekere diẹ ju pẹlu awọn ijumọsọrọ telemedicine isanwo.
Lórí ẹ̀sẹ̀ ènìyàn tí ó ní ulcerative colitis.
relevance score : -100.0%
ReferencesPyoderma gangrenosum jẹ ipo awọ ti o ṣọwọn ti o fa awọn ọgbẹ irora pẹlu awọn eti pupa tabi purplish. O ti pin si bi arun iredodo, ó sì jẹ́ apá kan ti ẹgbẹ kan tí a ń pè ní awọn dermatoses neutrophilic. Idi ti Pyoderma gangrenosum jẹ́ idiju, pẹ̀lú àwọn ìṣòro ní innate immunity àti adaptive immunity ní àwọn ènìyàn tí ó ní genetic predisposition. Láìpẹ́, àwọn oníwádìí ti dojú kọ́ lori hair follicle gẹ́gẹ́ bí àyè ibẹrẹ tó pọ̀jù ti arun náà.
Pyoderma gangrenosum is a rare inflammatory skin disease classified within the group of neutrophilic dermatoses and clinically characterized by painful, rapidly evolving cutaneous ulcers with undermined, irregular, erythematous-violaceous edges. Pyoderma gangrenosum pathogenesis is complex and involves a profound dysregulation of components of both innate and adaptive immunity in genetically predisposed individuals, with the follicular unit increasingly recognized as the putative initial target.
Pyoderma gangrenosum is a rare inflammatory skin disease classified within the group of neutrophilic dermatoses and clinically characterized by painful, rapidly evolving cutaneous ulcers with undermined, irregular, erythematous-violaceous edges. Pyoderma gangrenosum pathogenesis is complex and involves a profound dysregulation of components of both innate and adaptive immunity in genetically predisposed individuals, with the follicular unit increasingly recognized as the putative initial target.
Pyoderma gangrenosum jẹ́ àìlera àwọ̀ tó ṣọ́wọn tí ó ń fa irora tó pọ̀. Bí a kò tíì mọ̀ ìdí rẹ̀ ní kíkún, a ti rí i pé ó ní í ṣe pẹ̀lú iṣẹ́ àìlera tó pọ̀ síi ti àwọn sẹẹ́lì ajẹ́ṣàra kan. Itọju arun náà kì í ṣe rọrùn. A ní ọ̀pọ̀lọpọ̀ òògùn tó lè dín àkúnya ajẹ́ṣàra kù tàbí tún iṣẹ́ rẹ̀ ṣe. Lẹ́gbẹ̀ẹ́ àwọn wọ̀nyí, a tún ń fojú kọ́ àtìlẹ́yìn àtì ìṣètò àwọn ọ̀gbẹ́ àti iṣakoso irora. Corticosteroids àti cyclosporine máa ń jẹ́ yíyan àkọ́kọ́ fún itọju, ṣùgbọ́n ní báyìí, ìwádìí míì ti ń fojú kọ́ lílo àwọn itọju biologic bí inhibitors TNF-α. Àwọn onímọ̀-jìnlẹ̀ wọ̀nyí ti di ayanfẹ jùlọ, pàápàá jùlọ fún àwọn aláìsàn tí ó ní àìlera míì míì, wọ́n sì ń lò ó ní ìbẹ̀rẹ̀ ìṣètò arun náà.
Pyoderma gangrenosum is a rare neutrophilic dermatosis that leads to exceedingly painful ulcerations of the skin. Although the exact pathogenesis is not yet fully understood, various auto-inflammatory phenomena with increased neutrophil granulocyte activity have been demonstrated. Despite the limited understanding of the pathogenesis, it is no longer a diagnosis of exclusion, as it can now be made on the basis of validated scoring systems. However, therapy remains a major multidisciplinary challenge. Various immunosuppressive and immunomodulatory therapies are available for the treatment of affected patients. In addition, concomitant topical pharmacologic therapy, wound management and pain control should always be addressed. Corticosteroids and/or cyclosporine remain the systemic therapeutics of choice for most patients. However, in recent years, there has been an increasing number of studies on the positive effects of biologic therapies such as inhibitors of tumour necrosis factor-α; interleukin-1, interleukin-17, interleukin-23 or complement factor C5a. Biologics have now become the drug of choice in certain scenarios, particularly in patients with underlying inflammatory comorbidities, and are increasingly used at an early stage in the disease rather than in therapy refractory patients.
Pyoderma gangrenosum is a rare neutrophilic dermatosis that leads to exceedingly painful ulcerations of the skin. Although the exact pathogenesis is not yet fully understood, various auto-inflammatory phenomena with increased neutrophil granulocyte activity have been demonstrated. Despite the limited understanding of the pathogenesis, it is no longer a diagnosis of exclusion, as it can now be made on the basis of validated scoring systems. However, therapy remains a major multidisciplinary challenge. Various immunosuppressive and immunomodulatory therapies are available for the treatment of affected patients. In addition, concomitant topical pharmacologic therapy, wound management and pain control should always be addressed. Corticosteroids and/or cyclosporine remain the systemic therapeutics of choice for most patients. However, in recent years, there has been an increasing number of studies on the positive effects of biologic therapies such as inhibitors of tumour necrosis factor-α; interleukin-1, interleukin-17, interleukin-23 or complement factor C5a. Biologics have now become the drug of choice in certain scenarios, particularly in patients with underlying inflammatory comorbidities, and are increasingly used at an early stage in the disease rather than in therapy refractory patients.
